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Right bundle branch block

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Instructors' Collection ECG: Wide Complex Tachycardia

Fri, 02/05/2021 - 21:11 -- Dawn

This pair of ECGs feature one of our recurring themes:  wide-complex tachycardia (WCT). It is a fascinating topic, as tachycardia has many causes and many mechanisms, and wide QRS also has many causes, with the mechanism being slow conduction through the ventricles. 

Sometimes, it is not possible to diagnose the true origin of a WCT from one ECG, or even serial ECGs.  Is the tachycardia due to increased sympathetic activity (fear, dehydration, exercise, hypoxia, hypovolemia, etc.)?  Or is the fast rate due to reentry, where one impulse gets “caught” in a loop, repeating itself rapidly, and depolarizing the myocardium with each pass?  What is the location of the pacemaker that is responsible for the rhythm?  Is it a supraventricular rhythm that has suffered an intraventricular conduction delay, widening the QRS?  Or is the rhythm originating in a ventricular pacemaker, without the ability to travel on the fast highway that is the intraventricular conduction system? 

If you or your students work in an acute care setting, such as pre-hospital or emergency department, you may not be with the patient long enough or be able to conduct enough tests to determine without a doubt the answers to the above questions.  Some WCTs cause such severe symptoms that they must be dealt with quickly, to avoid rapid deterioration to ventricular fibrillation.  For that reason, there is a widely-accepted rule for WTC treatment:


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Second-degree AV Block, Type II

Tue, 12/08/2020 - 13:47 -- Dawn

The patient:  Unfortunately, we no longer have information on this patient, other than the fact that she went to the OR for a permanent pacemaker implantation.

The ECG:  The atrial rate (P waves) is 99 beats per minute. The P waves are regular and all alike (NSR). The ventricular rate (QRS complexes) is 33 bpm, and the QRS complexes are regular and all alike. The PR intervals, when A-V conduction occurs, are 162 ms (.16 seconds) and all alike. The QRS complexes are wide, at 122 ms (.12 seconds). There is right bundle branch block, but no left hemiblock, as the frontal plane axis is normal. The QTc is prolonged at 549 ms.  Many ST segments on this ECG have a “flat” appearance, rather than the normal concave up shape.

The failure of 2 out of every 3 P waves to conduct indicates a second-degree AV block. Type I is a block of the AV node, with progressive prolongation of the PR interval until ONE P wave fails to conduct. Type II AV block is a block of the intraventricular conduction system. Clues that a second-degree AV block is Type II include:

·        The PR intervals are all alike.

·        More than one consecutive P wave is not conducted.

·        A P wave that is NOT in the refractory period of the preceding beat is not conducted.

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Right Bundle Branch Block and More

Sat, 08/22/2020 - 15:33 -- Dawn

The Patient:    These tracings are taken from a 75-year-old man who became weak while playing golf on a very hot day.  He was pale and diaphoretic.  He was hypotensive, but we do not know his BP reading. He denies chest pain or discomfort. The patient reported a history of lung cancer and hypertension. We have no other history, and unfortunately, no follow-up information.

ECG Number 1:           The first ECG shows the standard 12 leads.  The rhythm is sinus with frequent appearances of PAC couplets.  The sinus rate varies slightly from about 76 bpm to 68 bpm, tending to slow a bit after the premature atrial contractions.  There is a right bundle branch block, and the QRS duration is about .12 seconds (120 ms). The PR interval is slightly log at 223 ms.  We do not know what medications the patient is on, and we do not have an older ECG for comparison.

There are some interesting, if subtle, changes worth mentioning.  The QRS complexes in most leads are fragmented.  That is, they have notching in the terminal S or R waves that is not due to the bundle branch block. This can be a sign of scarring, and can also be considered an equivalent to a pathological Q wave.  Speaking of pathological Q waves, they are seen in the inferior leads, II, III, and aVF.  There are also prominent, though not large Q waves in V4 through V6, leads which normally do not have them. All this points to scarring and possibly long-term coronary artery disease, with possible old M.I.  In addition, the ST segments are not entirely normal.  There is ST depression in the inferior and low lateral leads, a little ST elevation in aVL.  Also, the SHAPES of the ST segments tend to be straight throughout the ECG, instead of the usual curved (concave up) appearance.

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High-grade AV Block With Profound Bradycardia

Thu, 06/04/2020 - 14:24 -- Dawn

If you are an ECG instructor, you probably carefully choose ECGs to illustrate the topic you are teaching. One of the reasons for the existence of the ECG Guru website is our desire to provide lots of such illustrations for you to choose from.

Sometimes, though, an ECG does not clearly illustrate one specific dysrhythmia well, because the interpretation of the ECG depends on so many other factors.  In order to get it “right”, we would need to know information about the patient’s history, presentation, lab results, or previous ECGs. We might need to see the ECG done immediately before or after the one we are looking at.  Some ECG findings must ultimately be confirmed by an electrophysiology study before we can know for sure what is going on.

For those of us who are “ECG nerds”, it can be fun to debate our opinions and even more fun to hear from wiser, more advanced practitioners about their interpretations.

My belief, as a clinical instructor, is that we must teach strategies for treating the patient who has a “controversial” ECG that take into account the level of the practitioner, the care setting, and the patient’s hemodynamic status.  In some settings, it might be absolutely forbidden for a first-responder to cardiovert atrial fibrillation, for example.  But atrial fib is routinely cardioverted under controlled conditions in hospitals.  The general rule followed by emergency providers that “all wide-complex tachycardias are v tach until proven otherwise” has no doubt prevented deaths in situations where care providers did not agree on the origin of the tachycardia.

The ECG:    We do not have much patient information to go with this ECG, just that it is from a 71-year-old woman who developed severe hypotension and lost consciousness, but was revived with transcutaneous pacing.   Here is what we do know about this ECG:

·        There are regular P waves, at a rate of about 39 bpm (sinus bradycardia).

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Shark Fin Pattern

Mon, 01/27/2020 - 21:54 -- Dawn

The Patient:  This ECG is from a 59-year-old woman who was found by the EMS crew to be unresponsive, with agonal respirations at about 6 breaths per minute. Her pulse was thready at the carotid, and absent peripherally. Her skin was pale, cool, and mottled.  Her BP via the monitor is 81/40, peripheral pulses not being palpable.  An initial rhythm strip showed sinus rhythm at 75 bpm with right bundle branch block and ST elevation.

The patient’s husband gave a history of “difficulty breathing” since sometime this morning, alcohol dependence, hypertension, tobacco use, and insomnia. He said she had been drinking heavily for several weeks.

She was immediately ventilated and intubated, and an intraosseous infusion line established.  A12-lead ECG was done, and it showed a dramatic change in the rhythm and ST segments over the initial strip. She was transported to a nearby hospital with CPR support. She achieved return of spontaneous circulation (ROSC) at the Emergency Department, after having three doses of epinephrine.  Follow up with the ED physician revealed that the patient had suffered a massive gastrointestinal bleed.  This patient, due to loss of a critical amount of blood, had low blood pressure and very poor perfusion, which resulted in damage to her heart (and possibly other organs as well). I do not have further follow up, but will update this if I receive more information. 

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Tachycardia In An Unresponsive Patient

Tue, 08/20/2019 - 20:48 -- Dawn

 The Patient     This ECG was obtained from a 28-year-old woman who was found in her home, unresponsive.  She was hypotensive at 99/35.  No one was available to provide information about past medical history or the onset of this event.

Before you read my comments, pause to look at the ECG and see what YOU think.  We would welcome comments below from all our members!

The ECG     This ECG is quite challenging, as it illustrates the helpfulness of ECG changes in patient diagnosis, and also points out how important clinical correlation is when the ECG suggests multiple different problems. Forgive me in advance, but there is a lot to say about this ECG.

The heart rate is 148 bpm, and the rhythm is regular, although not perfectly. P waves are not seen, even though the ECG machine gives a P wave axis and PR interval measurement. The rate is fast enough to bury the P waves in the preceding T waves, especially if there is first-degree AV block. Differential dx: sinus tachycardia, PSVT, atrial flutter. The very slight irregularity points more towards sinus tachycardia.  The rate of nearly 150 suggests atrial flutter with 2:1 conduction, but the only lead that looks remotely like it has flutter waves is V2. The lack of an onset or offset of the rhythm makes it difficult to diagnose PSVT with any certainty.

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Bifascicular Block With First-degree AVB

Wed, 04/24/2019 - 21:29 -- Dawn
The Patient  This ECG was obtained from an 80-year-old man with a past medical history of hypertension, diabetes, chronic obstructive pulmonary disease, hyperlipidemia, chronic kidney disease, and heart failure with preserved ejection fraction (HFpEF).


He presented to the hospital with a complaint of shortness of breath, and was determined to have an exacerbation of his COPD in the setting of a viral infection.  He was treated with breathing treatments and steroids, and was discharged home in improved condition.

The ECG   There is a sinus rhythm at 80 bpm.  The QRS complex is wide at .18 seconds (180 ms). The PR interval is slightly prolonged at .24 seconds (240 ms), which is first-degree AV block. There is right bundle branch block (QR in V1 and rS in Leads I and V6 with a wide QRS).  There is also a left posterior fascicular block (also called hemiblock), recognized by the right axis deviation (III is taller than aVF ).  This is bi-fascicular block, which can be chronic or acute.  There is very slight ST elevation with flattening in V1 and possibly V2.  In RBBB, “normal” T waves are directed opposite the terminal wave of the QRS.  V3 should, then, have inverted T waves. So, the upright T wave in this patient could be considered to be equivalent to an inversion in a normal ECG.  V4 through V6 have biphasic T waves, which is not normal for RBBB.  Because we do not have an old ECG, we don’t know which, if any, of these changes are chronic.  With this patient’s past medical history, it is possible for any of them to be pre-existing.

I will admit that, when I first saw this ECG, the V1 rhythm strip at the bottom looked as though there were regular P waves at a rate of about 220-240, with one buried in each QRS and one in each T wave. In scrutinizing all the other leads, I cannot find evidence for an underlying atrial tachycardia or atrial flutter, so it is probably a coincidence that the P and T “march out” with the assumption of a hidden P wave in the QRS.

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Bifascicular Block

Fri, 11/16/2018 - 14:35 -- Dawn

This ECG is from a 77 year old woman who was brought to the Emergency Department by EMS. She was found to be suffering from sepsis.

ECG Interpretation      The ECG shows the expected sinus tachycardia at 123 beats per minute.  There is significant baseline artifact, of the type usually seen with muscle tension.  The artifact makes it difficult to assess P waves and PR intervals.


What we do see is RIGHT BUNDLE BRANCH BLOCK and LEFT ANTERIOR HEMIBLOCK, also called LEFT ANTERIOR FASCICULAR BLOCK.  Together, these are called BIFASCICULAR BLOCK.  Most people have three main fascicles in the interventricular conduction system:  the right bundle branch and the two branches of the left bundle branch, the anterior-superior fascicle and the posterior-inferior fascicle.  In bifascicular block, two of the three are blocked.

The ECG criteria for right bundle branch block are:

     *     wide QRS (> .12 seconds)


     *     rSR’ pattern in V1 .  (the initial R wave may be hard to see, but the QRS will be predominantly upright.

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Right Bundle Branch Block With Probable Previous M.I.

Sat, 09/08/2018 - 14:35 -- Dawn

This ECG was obtained from an 87-year-old man with chest discomfort.  We have no other clinical information.

ECG Interpretation   The rhythm is regular and fast, with P waves, at 95 beats per minute. So, it is normal sinus rhythm, but the rate is probably not “normal” for this patient.  The P waves are small, and difficult to see.  We suggest Lead I to best view the P waves in this example. This is a good opportunity to teach the value of evaluating rhythm strips in more than one simultaneous lead, as subtle features may not show up well in all leads.  There is a first-degree AV block, with a PR interval of 232 ms.

We see the right bundle branch block (RBBB) pattern: rSR’ in the right precordial leads (with a tiny q wave in V1, which is not typical of  RBBB).  The QRS is wide at 148 ms (.148 seconds).  The R prime (R’) represents the right ventricle depolarizing slightly after the left ventricle.  This terminal delay widens the QRS without affecting the depolarization or contraction of the left ventricle.  This delay can be seen in every lead, but is especially easy to see in Leads I and V6, where there is a wide little s wave.  It is normal for the T waves to be in a direction opposite that of the terminal wave (inverted in Leads V1 and III, for example.)

There is left axis deviation.  The causes of LAD are many.  It is not unusual for people with RBBB to also have a left anterior hemiblock (LAH), also called left anterior fascicular block.  The left anterior fascicle has the same blood supply as the right bundle branch.   LAH causes a frontal plane axis shift – instead of Lead II having the tallest QRS of the limb leads, Leads I and aVL will be the tallest upright QRS complexes of the six limb leads.  Lead II will be very small, or flat, or negative. However, the probability of pathological Q waves in the inferior leads offers a more likely explanation for the leftward axis shift.  The M.I. that would have caused these Q waves is old, as there are no acute ST changes.  It would, of course, help to know this patient’s history.

Right bundle branch block can make evaluating for ST segment elevation a bit tricky.  Occasionally, the terminal delay – especially in Leads III and aVF – can be mistaken for ST elevation.  The J points in this ECG all appear to be at the baseline, with no overt STEMI.


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Acute M.I. With Right Bundle Branch Block and Atrial Pacing

Wed, 01/24/2018 - 22:08 -- Dawn

This ECG was taken from a 78-year-old man who was experiencing chest pressure in the morning, after having left shoulder pain since the night before. He has a history of hypertension and hypercholesterolemia, and has an implanted pacemaker.

What does the ECG show?  The ECG shows an atrial paced rhythm, with two premature beats, beats number 5 and 12.  These are probably PVCs.  The patient has a functioning AV conduction system, so the paced atrial beats are conducting through the AV node and producing QRS complexes.  In the interventricular conduction system, the impulse encounters right bundle branch block. This causes each QRS to have an “extra” wave attached at the end, representing slightly delayed depolarization of the right ventricle.  Instead of an “rS” pattern in V1, for example, we see “rSR’ “.  The slight delay causes the QRS to be widened, as we are measuring the two ventricles separately, rather than synchronously.

There is definite ST segment elevation in V2 and V3, and the shape of the ST segment is straight, having lost it’s normal “concave upward” appearance.  In an ECG taken three minutes later, the STE extends to V4.

Do the pacemaker or the right bundle branch block prevent us from diagnosing an ST-elevation M.I.?  The answer to that is a resounding “NO!” Pacemakers can sometimes make it difficult to assess ST elevation because ventricular pacing causes ST segment changes.  Pacing the right ventricle causes a depolarization delay in the left ventricle as the impulse travels “cell to cell” across the LV.  This means an RV-paced beat will resemble a PVC from the RV.  When LV depolarization is altered, repolarization will also be altered, causing ST elevation in leads with negative QRS complexes, and ST depression is leads with upright QRSs. These are called discordant ST changes. These changes are proportionate to the height or depth of the QRS, with very minimal or no ST changes in leads with short or biphasic QRS complexes.  We don’t have to worry about that in this situation – the pacemaker is not pacing the ventricles.


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